The functional anatomy of caveolae across cell types

Caveolae are 50-100nm, cholesterol- and sphingolipid-enriched invaginations of the plasma membrane, assembled from caveolin and cavin proteins. They are not generic vesicles distributed equally across mammalian tissues, but cell-type-specific membrane organelles whose abundance, molecular composition and physiological roles vary widely. This review synthesises the evidence for caveolae across the cellular landscape and treats distribution, signalling and disease as a single axis. Endothelial cells, adipocytes and muscle cells represent the highest-density systems, where caveolae support transcytosis, membrane tension buffering, lipid handling, contractile signalling and ion-channel organisation. Fibroblasts are also a well-supported non-endothelial model, with genetic and functional evidence linking caveolin-1 and cavin-1 to caveola formation, integrin mechanosensing, matrix production and fibrosis; by contrast, direct evidence for fibrocytes remains sparse. In epithelia, glia, immune cells, stromal cells and cancer cells, caveolin expression must be distinguished from the verified presence of bona fide caveolae. This distinction is particularly important for telocytes, mature neurons, lymphocytes and tumour cells, where caveolin-based markers, non-caveolar scaffolds and context-dependent loss of cavin proteins complicate interpretation. Disease phenotypes mirror this cellular specificity: mutations or dysregulation lead to muscle caveolinopathies, pulmonary arterial hypertension, lipodystrophy, vascular and blood-brain barrier dysfunction, fibrosis, altered host-pathogen entry, and cancer phenotypes. A cell-type-resolved view therefore complements mechanism-centred accounts of caveola mechanics and helps explain why one caveolin-cavin module can generate divergent physiological and pathological outcomes.